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吞噬细胞产生的自由基:在细胞毒性和炎症中的作用。

Phagocyte-produced free radicals: roles in cytotoxicity and inflammation.

作者信息

McCord J M, Wong K

出版信息

Ciba Found Symp. 1978(65):343-60. doi: 10.1002/9780470715413.ch19.

Abstract

The production of superoxide free radical, O2-, by metabolically activated phagocytes results in damage to the phagocyte which is manifested by the premature death of the cell in vitro. The cytotoxic agent appears to be formed by the reaction of superoxide with hydrogen peroxide, and is thought to be hydroxyl radical or a secondary radical thereof. In vivo two animal models of induced inflammation also appear to be largely dependent on superoxide production by phagocytes for the development of tissue damage manifested as oedema. Intravenously administered superoxide dismutase shows anti-inflammatory activity in these models, but only when so derivatized that it can remain in the circulation for longer periods of time. Catalase, or a catalase derivative, on the other hand, shows no anti-inflammatory activity in vivo.

摘要

代谢激活的吞噬细胞产生超氧阴离子自由基O₂⁻,会导致吞噬细胞受损,这在体外表现为细胞过早死亡。细胞毒性剂似乎是由超氧阴离子与过氧化氢反应形成的,被认为是羟基自由基或其二级自由基。在体内,两种诱导炎症的动物模型在很大程度上似乎也依赖吞噬细胞产生超氧阴离子来引发组织损伤,表现为水肿。在这些模型中,静脉注射超氧化物歧化酶具有抗炎活性,但前提是要进行衍生化处理,使其能在循环中保留更长时间。另一方面,过氧化氢酶或过氧化氢酶衍生物在体内没有抗炎活性。

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